Chronic diseases involving tissue fibrosis are a major health burden, resulting in irreversible damage to the fibrotic organ and the need for transplant. In most cases of fibrosis, disease progression involves repeated cycles of inflammation, followed by epithelial injury and repair, which in turn, causes scarring and tissue malfunction. The major molecule responsible for promoting tissue fibrosis is transforming growth factor beta (TGF-β), a cytokine normally released in response to injury that stimulates wound repair. However, overproduction of TGF-β can be damaging, and this phenomenon is consistently observed in fibrotic diseases, suggesting that TGF-β dysregulation can act as a driver of disease.